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Blood, 1 August 2006, Vol. 108, No. 3, pp. 947-955. Prepublished online as a Blood First Edition Paper on April 13, 2006; DOI 10.1182/blood-2005-12-4812. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-12-4812v1 108/3/947    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Skoberne, M. Articles by Bhardwaj, N. Search for Related Content PubMed PubMed Citation Articles by Skoberne, M. Articles by Bhardwaj, N. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 6, 2005 Accepted February 27, 2006 The apoptotic cell receptor CR3, but not v5, is a regulator of human dendritic cell immunostimulatory function Mojca Skoberne, Selin Somersan, Wanda Almodovar, Tuan Truong, Kseniya Petrova, Peter M Henson, and Nina Bhardwaj* NYU School of Medicine, New York, NY, USA Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA * Corresponding author; email: bhardn02{at}med.nyu.edu. Dendritic cells (DCs) that capture apoptotic cells (AC) in the steady-state mediate peripheral tolerance to self-antigens. ACs are recognized by an array of receptors on DCs, the redundancy of which is not completely defined. We made use of an AC surrogate system to address the individual roles of the v5 and complement receptors (CR) in the phagocytosis and induction of immunity. CR3 and CR4, while substantially less efficient than v5 in internalizing ACs, initiate signals that render DCs tolerogenic. Responding T cells show impaired proliferation and IFN production, and subsequently die by apoptosis. While tolerogenic DCs are not induced via v5, co-ligation of CR3 and v5 maintains the DCs[[rad]] tolerogenic profile. This immunomodulatory role, however, is countered by a significant inflammatory stimulus such as bacterial infection. Overall, our data suggest that under steady state conditions, signaling via CRs predominates to render DCs tolerogenic. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Spirig, C. van Kooten, C. Obregon, L. Nicod, M. Daha, and R. Rieben The Complement Inhibitor Low Molecular Weight Dextran Sulfate Prevents TLR4-Induced Phenotypic and Functional Maturation of Human Dendritic Cells J. Immunol., July 15, 2008; 181(2): 878 - 890. [Abstract] [Full Text] [PDF] I. M. Olazabal, N. B. Martin-Cofreces, M. Mittelbrunn, G. Martinez del Hoyo, B. Alarcon, and F. Sanchez-Madrid Activation Outcomes Induced in Naive CD8 T-Cells by Macrophages Primed via "Phagocytic" and Nonphagocytic Pathways Mol. Biol. Cell, February 1, 2008; 19(2): 701 - 710. [Abstract] [Full Text] [PDF] E. M. Behrens, U. Sriram, D. K. Shivers, M. Gallucci, Z. Ma, T. H. Finkel, and S. Gallucci Complement Receptor 3 Ligation of Dendritic Cells Suppresses Their Stimulatory Capacity J. Immunol., May 15, 2007; 178(10): 6268 - 6279. [Abstract] [Full Text] [PDF] P. Sen, M. A. Wallet, Z. Yi, Y. Huang, M. Henderson, C. E. Mathews, H. S. Earp, G. Matsushima, A. S. Baldwin Jr, and R. M. Tisch Apoptotic cells induce Mer tyrosine kinase-dependent blockade of NF-{kappa}B activation in dendritic cells Blood, January 15, 2007; 109(2): 653 - 660. [Abstract] [Full Text] [PDF]

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